We have found in our previous studies that the hypofunction of the aged brain is caused by decreased synaptic transmission, and that the diminished transmission is due to decreased CaィイD12+ィエD1influx through voltage-dependent calcium channels. Based on these findings, we aimed to enhance the synaptic transmission of the aged brain in this study. (1) Gangliosides enriched on synaptic membranes were examined for their effects on CaィイD12+ィエD1influx. Ganglioside, GM1 or GQ1b, increased the depolarization-induced acetylcholine release from synaptosomes. This effect was proved to be due to enhanced efficacy of calcium channels. (2) Long-term potentiation as a marker of synaptic plasticity was enhanced by ganglioside GM1 or GQ1b. (3) In the attempt to apply the ganglioside effects on human cases, sialyl compounds, ganglioside analognes, of smaller molecular weight were speculated to be superior to natural gangliosides. Sialyl cholesterol was found to enhance the synaptic transmission.